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Prostate cancer

Mutational consequences

Nature Reviews Cancer volume 12, pages 450–451 (2012)Cite this article

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Grasso et al. conducted exome sequencing of 50 lethal, heavily pretreated castration-resistant prostate cancers (CRPCs), as well as 11 treatment-naive, high-grade, localized prostate cancers. To identify recurrent DNA copy number changes that might be driving lesions in CRPC, the authors analysed this exome data, as well as an independent array comparative genomic hybridization data set. One peak of copy number loss contained chromodomain helicase DNA-binding protein 1 (CHD1), which encodes a chromatin-remodelling enzyme. Further analysis of data from several studies (954 prostate cancers) found that 5.2% had CHD1 loss by deletion or mutation; most lacked ETS gene family fusions (which are commonly involved in prostate cancer) and so may represent a novel prostate cancer subtype.

The authors looked for aberrations in ETS genes, and found a mutation in a conserved residue (R437C) in ETS2 in an ETS-fusion-negative tumour. Migration, invasion and proliferation of VCaP prostate cancer cells were suppressed by expression of wild-type ETS2, but promoted by ETS2R437C, indicating that ETS2 might be a tumour suppressor that is deregulated by mutation.

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ORIGINAL RESEARCH PAPERS

  1. Barbieri, C. E. et al. Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer. Nature Genet. 20 May 2012 (doi:10.1038/ng.2279)

  2. Grasso, C. S. et al. The mutational landscape of lethal castration-resistant prostate cancer. Nature 20 May 2012 (doi:10.1038/nature11125)

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  1. Sarah Seton-Rogers
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Seton-Rogers, S. Mutational consequences. Nat Rev Cancer 12, 450–451 (2012). https://doi.org/10.1038/nrc3303

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